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首页> 外文期刊>Molecular Microbiology >Identification and characterization of spdR mutations that bypass the BsgA protease-dependent regulation of developmental gene expression in Myxococcus xanthus.
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Identification and characterization of spdR mutations that bypass the BsgA protease-dependent regulation of developmental gene expression in Myxococcus xanthus.

机译:spdR突变的鉴定和表征,该突变绕过了黄色粘球菌中BsgA蛋白酶依赖性的发育基因表达调控。

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The BsgA protease of Myxococcus xanthus is an intracellular protease closely related to the Lon protease of Escherichia coli. BsgA is required for normal levels of developmentally induced gene expression. In this report, we describe the identification of mutations that suppress the developmental defect of bsgA mutants. These mutations localized to the spdR gene (suppressor protease deficiency regulator) that appears to play a role in the regulation of early developmental gene expression. Mutations in spdR fully restored the ability of a bsgA mutant to form fruiting bodies and spores and, with one exception, restored the expression of several development-specific lacZ fusions. spdR mutants exhibited characteristic phenotypic properties including increased expression of the development-specific tps gene during vegetative growth, formation of fruiting bodies and spores on semi-rich nutrient medium and completion of starvation-induced development in a shorter time period than wild-type strains. The spdR locus was cloned and sequenced and found to encode a member of the NtrC family of two-component transcriptional regulators. One interpretation of these data is that SpdR acts, directly or otherwise, to regulate developmental gene expression negatively and that the BsgA protease is required to relieve this inhibitory effect at the onset of development. However, Western immunoblot analysis indicated that SpdR is present at a relatively constant level during growth and early development in both wild-type and BsgA protease-deficient cells. This finding suggests that BsgA does not function to degrade SpdR at the onset of development.
机译:黄褐粘球菌的BsgA蛋白酶是与大肠杆菌的Lon蛋白酶紧密相关的细胞内蛋白酶。 BsgA是正常水平的发育诱导基因表达所必需的。在此报告中,我们描述了抑制bsgA突变体发育缺陷的突变的鉴定。这些突变定位于似乎在早期发育基因表达的调节中起作用的spdR基因(抑制剂蛋白酶缺乏调节剂)。 spdR中的突变完全恢复了bsgA突变体形成子实体和孢子的能力,并且除了一个例外,恢复了几种发育特异性lacZ融合体的表达。 spdR突变体表现出特征性的表型特性,包括在营养生长过程中发育特异性tps基因的表达增加,在半富营养培养基上形成子实体和孢子以及在比野生型菌株更短的时间内完成饥饿诱导的发育。克隆并测序了spdR基因座,发现该基因编码了NtrC家族的两组分转录调节子家族。这些数据的一种解释是SpdR直接或以其他方式负调控发育基因的表达,并且需要BsgA蛋白酶在发育开始时减轻这种抑制作用。但是,Western免疫印迹分析表明,SbpR在野生型和BsgA蛋白酶缺陷型细胞的生长和早期发育过程中以相对恒定的水平存在。这一发现表明,BsgA不能在发育开始时降解SpdR。

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